Updated on 2026/08/16

写真a

 
Bessho Ryoichi
 
Organization
School of Medicine Medical Course Clinical Medicine Internal Medicine [Division of Endocrine,Metabolic, Collagen disease ]
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Degree

  • Ph.D. (Medicine) ( 2020.3   Asahikawa Medical College )

Research Interests

  • Diabetic Nephropathy

  • Cellular Metabolism

  • Mitochondria

Research Areas

  • Life Science / Cell biology  / Cellular Biology

  • Life Science / Nephrology  / Nephrology

  • Life Science / Metabolism and endocrinology  / Endocrinology and Metabolism

Education

  • Asahikawa Medical College   Graduate School of Medical Research

    2015.4 - 2020.3

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    Country： Japan

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  • Asahikawa Medical College   Department of Medicine

    2009.4 - 2015.3

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    Country： Japan

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Research History

  • Asahikawa Medical College   Division of Endocrinology, Metabolism and Reumatology, Department of Internal Medicine   Assistant Professor

    2026.7

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  • Vanderbilt University Medical Center   Division of Nephrology and Hypertension   Postdoctoral Research Fellow

    2024.4 - 2026.5

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    Country：United States

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  • Vanderbilt University Medical Center   Division of Nephrology and Hypertension   Visiting Research Fellow

    2023.4 - 2024.3

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    Country：United States

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  • Asahikawa Medical University Hospital   Department of Internal Medicine   Clinical Fellow

    2020.11 - 2023.3

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    Country：Japan

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  • Asahikawa Medical University Hospital   Department of Internal Medicine   Senior Resident and Clinical Fellow

    2017.4 - 2020.3

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    Country：Japan

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  • Asahikawa Medical University Hospital   Junior Resident

    2015.4 - 2017.3

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    Country：Japan

    Notes：Cooperating hospital; National Hospital Organization Asahikawa Medical Center

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Professional Memberships

  • Japanese Society of Nephrology

    2022

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  • Japan Thyroid Association

    2020

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  • The Japan Diabetes Society

    2017

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  • The Japan Endocrine Society

    2017

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  • The Japanese Society of Internal Medicine

    2015

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Committee Memberships

  •   日本内分泌学会, JES We Can（男女共同参画推進委員会）  

    2026.7   

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  • The Japan Endocrine Society   Gender Equality Promotion Committee; Japan Endocrine Society Women Endocrinologists Association (JES We Can)  

    2022.4 - 2023.3   

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    Committee type：Academic society

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  • The Japan Diabetes Society   The Committee to promote diversity of diabetes medical professionals and researchers  

    2021.4 - 2023.3   

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    Committee type：Academic society

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Papers

  • Regional metabolic analysis of structurally preserved kidney slices by ex vivo respirometry. International journal

    Ryoichi Bessho, Olena Davidoff, Hanako Kobayashi, Volker H Haase

    American journal of physiology. Renal physiology   329 ( 6 )   F796-F808   2025.12

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    Language：English   Publishing type：Research paper (scientific journal)  

    A comprehensive spatial analysis of kidney metabolism is essential for advancing knowledge of both normal kidney physiology and pathophysiology. The kidney exhibits marked regional differences in bioenergetic demands and substrate utilization, reflecting the distinct functional profiles of each nephron segment. To complement existing approaches with freshly isolated tubules or primary cell cultures, we established and validated an ex vivo respirometry method using structurally preserved kidney slices on a Seahorse XFe24 platform. This protocol avoids tissue disruption or enzymatic digestion and enables simultaneous, region-specific measurements of metabolic fluxes in the cortex, outer medulla, and inner medulla. It provides an integrated readout of the metabolic properties of the cell types present within each anatomical region. We demonstrate the utility of this approach through proof-of-principle studies that profile region-specific metabolic fluxes under hyperglycemic conditions in a mouse model of obesity and type 2 diabetes, as well as the metabolic alterations that accompany the transition from acute ischemic injury to chronic kidney disease. Furthermore, to highlight its relevance for therapeutic discovery, we applied this method to assess the impact of pharmacological hypoxia-inducible factor activation on regional kidney bioenergetics. In summary, this protocol advances the study of kidney metabolism by providing a robust platform for region-specific analysis of kidney respiration and bioenergetics and holds promise for accelerating the development of novel therapies targeting metabolic pathways in kidney disease.NEW & NOTEWORTHY Assessment of regional metabolism in kidney tissue is crucial for understanding normal physiology and disease. We have developed a robust ex vivo method to measure respiration in structurally preserved kidney slices using a metabolic flux analyzer. This approach enables analysis of metabolic fluxes and substrate utilization in the kidney cortex, outer medulla, and inner medulla while maintaining tissue architecture, providing region-specific insights into kidney metabolism with broad applications in disease modeling and therapeutic discovery.

    DOI： 10.1152/ajprenal.00157.2025

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  • インスリン抵抗性糖尿病と無月経の治療により改善したHAIR-AN症候群の1例

    池田 愛梨, 松尾 梨沙, 岸部 麻里, 別所 瞭一, 滝山 由美, 水無瀬 学, 野村 和加奈, 山本 明美

    皮膚科の臨床   67 ( 13 )   1785 - 1788   2025.12

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    Language：Japanese   Publisher：金原出版(株)  

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  • Rac1 promotes proximal tubule kidney repair by coupling the actin cytoskeleton to mitochondrial function. International journal

    Olga M Viquez, Meiling Melzer, Shensen Li, Matthew Tantengco, Xinyu Dong, Eric Sha, Jeffery Huang, Evan S Krystofiak, Rachel C Hart, Wentian Luo, Christian Warren, Al-Borhan Bayazid, Richard Zhang, Ryoichi Bessho, Volker H Haase, Cord Brakebusch, Takanari Inoue, Craig Brooks, Matthew H Wilson, Andrew S Terker, Juan P Arroyo, Ambra Pozzi, Roy Zent, Fabian Bock

    Proceedings of the National Academy of Sciences of the United States of America   122 ( 47 )   e2504565122   2025.11

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    The kidney proximal tubule (PT) is a specialized polarized epithelium that functions as a high capacity resorptive machine. PT cells are exquisitely sensitive to ischemia due to their high metabolic rate. The small GTPase Rac1 regulates epithelial function by promoting polarity through its effects on the actin cytoskeleton. We show that Rac1, in the setting of the recovery of the PT from ischemic injury, plays a critical role in reconstituting cellular bioenergetics by promoting actin cytoskeleton formation around damaged mitochondria. This mechanism removes damaged mitochondria through mitophagy and preserves PT metabolic capacity and reabsorption function. Loss of Rac1 causes intracellular lipid accumulation, energy depletion, and PT cell atrophy. Thus, Rac1 promotes the repair of PT cells by enhancing mitochondrial bioenergetics, rather than by regulating cell polarity via a mechanism that links the actin cytoskeleton to metabolic demands and cell morphology.

    DOI： 10.1073/pnas.2504565122

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  • Role of metallothionein 3 in diabetic nephropathy via interplay with HIF-1α.

    Yuri Takiyama, Yumi Takiyama, Takao Takiyama, Ryoichi Bessho, Hiroya Kitsunai, Akira Takasawa, Hiroshi Nomoto

    Diabetology international   16 ( 4 )   779 - 800   2025.10

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    UNLABELLED: Metallothioneins (MTs) are a cysteine-rich protein that scavenges reactive oxygen species. Hypoxia is involved in the progression of diabetic nephropathy (DN) and aggravates oxidative stress. Hypoxia dramatically induced MT3, whereas induced around twofold increment in MT2, but inhibited MT1 in human renal proximal tubular epithelial cells (HRPTECs). Given that the role of MT3 in DN remains unclear, we explored the involvement of MT3 in DN. Microarray analysis also identified MT3-regulated candidate genes, including ceruloplasmin (CP) and cytochrome b reductase 1 (CYBRD1), as well as FGF-Klotho (KL)-FGFR complexes in HRPTECs. Hypoxia significantly induced MT3 expression through HIF-1-dependent mechanisms, and MT3 small interfering RNA (siRNA) decreased CP, CYBRD1, and KL expression under hypoxic conditions. In humanized MT3-BACTg mice, except HIF-1α, diabetes significantly increased the expression of MT3, CP, CYRBD1, FGFR2, and KL in the renal cortex in MT3-BACTg mice. Diabetic MT3-BACTg mice presented more severely damaged mitochondria in proximal tubules than their wild-type littermates did, accompanied with peritubular capillary obstruction by swollen endothelial cells. Moreover, the proximal tubules-specific overexpression of MT3 in mice (MT3Tg) represented no overlap in the protein expression between MT3 and HIF-1α in diabetic kidney. Accordingly, MT3 siRNA significantly augmented HIF-1α protein and HIF1A in HRPTECs. Finally, MT3 expression in the renal tubulointerstitium was positively correlated with the glomerular filtration rate (GFR) in DN subjects by data from Nephroseq. In conclusion, these results showed that there might be a unique interplay between MT3 and HIF-1α in diabetic kidney of to regulate hypoxia-induced HIF-1α expression. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13340-025-00840-y.

    DOI： 10.1007/s13340-025-00840-y

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  • Dehydration promotes intracellular lipid synthesis and accumulation. International journal

    Joshua S Carty, Jazlyn Selvasingh, Yvonne Zuchowski, Hyuck-Jin Nam, Clothilde Pénalva, Gayani Nanayakkara, Erin Q Jennings, Kelsey Voss, Edith T Adame, John T Tossberg, Wei Sheng Yap, Meiling Melzer, Olga Viquez, A Scott McCall, Elizabeth R Piotrowski, Ryoichi Bessho, Shirong Cao, Katrina L Leaptrot, Alexandra C Schrimpe-Rutledge, Simona G Codreanu, Stacy D Sherrod, John A McLean, Jonathan B Trapani, Matthew A Cottam, Ma Wan, Deepti Shrivastava, Don Delker, Matthew H Wilson, Clinton M Hasenour, Louise Lantier, Irene Chernova, Jamey D Young, Volker H Haase, Jose Pablo Vazquez-Medina, Dylan K Kosma, Peter Kim, Jean-Philippe Cartailler, Mingzhi Zhang, Roy Zent, Raymond C Harris, Jason A Watts, Andrew S Terker, Fabian Bock, Jeffrey C Rathmell, Aylin R Rodan, Juan P Arroyo

    bioRxiv : the preprint server for biology   2025.8

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    Lipids can be considered a water reservoir used to offset dehydration stress as their oxidation by the mitochondria generates water. However, whether dehydration directly regulates lipid synthesis is unknown, which is the focus of this study. We found that dehydration stress decreases cellular oxygen consumption, increases intracellular lipid synthesis, and favors glutamine oxidation as a carbon precursor for lipid synthesis via remodeling mitochondrial metabolism. These findings provide a mechanism whereby cellular dehydration leads to intracellular lipid accumulation, functionally linking water availability to lipid storage.

    DOI： 10.1101/2025.08.07.669190

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  • Disruption of mitochondrial electron transport impairs urinary concentration via AMPK-dependent suppression of aquaporin 2. International journal

    Joshua S Carty, Ryoichi Bessho, Yvonne Zuchowski, Jonathan B Trapani, Olena Davidoff, Hanako Kobayashi, Joseph T Roland, Jason A Watts, Andrew S Terker, Fabian Bock, Juan Pablo Arroyo, Volker H Haase

    JCI insight   9 ( 22 )   2024.11

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    Urinary concentration is an energy-dependent process that minimizes body water loss by increasing aquaporin 2 (AQP2) expression in collecting duct (CD) principal cells. To investigate the role of mitochondrial (mt) ATP production in renal water clearance, we disrupted mt electron transport in CD cells by targeting ubiquinone (Q) binding protein QPC (UQCRQ), a subunit of mt complex III essential for oxidative phosphorylation. QPC-deficient mice produced less concentrated urine than controls, both at baseline and after type 2 vasopressin receptor stimulation with desmopressin. Impaired urinary concentration in QPC-deficient mice was associated with reduced total AQP2 protein levels in CD tubules, while AQP2 phosphorylation and membrane trafficking remained unaffected. In cultured inner medullary CD cells treated with mt complex III inhibitor antimycin A, the reduction in AQP2 abundance was associated with activation of 5' adenosine monophosphate-activated protein kinase (AMPK) and was reversed by treatment with AMPK inhibitor SBI-0206965. In summary, our studies demonstrated that the physiological regulation of AQP2 abundance in principal CD cells was dependent on mt electron transport. Furthermore, our data suggested that oxidative phosphorylation in CD cells was dispensable for maintaining water homeostasis under baseline conditions, but necessary for maximal stimulation of AQP2 expression and urinary concentration.

    DOI： 10.1172/jci.insight.182087

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  • Efficacy of Alogliptin/Metformin Fixed-Dose Combination Tablets and Vildagliptin/Metformin Fixed-Dose Combination Tablets on Glycemic Control in Real-World Clinical Practice for the Patients with Type 2 Diabetes: A Multicenter, Open-Label, Randomized, Parallel Group, Comparative Trial. International journal

    Tomoe Abe, Yasutaka Takeda, Ichiro Sakuma, Mizuho Okada, Ayaka Kurigaki, Ryoichi Bessho, Mao Sato, Hiroya Kitsunai, Yumi Takiyama, Masaru Sakurai

    Metabolic syndrome and related disorders   22 ( 9 )   651 - 660   2024.11

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    Background: This study was aimed to compare the efficacy of two combination tablets of dipeptidyl peptidase-4 (DPP-4) inhibitors and metformin with different dosages, alogliptin/metformin (AM) and vildagliptin/metformin (VM), on glycemic control in patients with type 2 diabetes (T2D). Methods: This was a prospective, multicenter, open-label, randomized, parallel group, comparative trial. After a run-in period of treatment with metformin alone, a total of 59 Japanese outpatients with T2D, aged 20-79 years with glycated hemoglobin (HbA1c) levels of 6.5%-10% were randomly assigned to 12-week AM treatment, alogliptin 25 mg/metformin 500 mg combination tablet orally once a day, or VM treatment, vildagliptin 50 mg/metformin 250 mg combination tablet orally twice a day. The primary endpoints were the changes in HbA1c and fasting plasma glucose (FPG) levels from baseline to week 12 between the two groups. Blinded intermittently scanned continuous glucose monitoring (isCGM) was performed between weeks 10 and 12. The incidence of adverse events during the study was also evaluated. Results: In all, 52 participants were analyzed. Significant decreases in HbA1c and FPG levels from baseline to week 12 were observed in both treatment groups. However, there were no significant differences between the AM and VM groups in the change in HbA1c level (-0.3% and -0.4%, P = 0.309) or the FPG level (-9.0 and -15.0 mg/dL, P = 0.789). The isCGM revealed that both treatments achieved the recommended glycemic target range. No adverse events, such as severe hypoglycemia, were observed in either group. Conclusions: We concluded that there were no significant differences in the efficacy of two combination tablets of DPP-4 inhibitors and metformin with different dosages on glycemic control in patients with T2D.

    DOI： 10.1089/met.2024.0127

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  • Disruption of nucleotide biosynthesis reprograms mitochondrial metabolism to inhibit adipogenesis. International journal

    Julia A Pinette, Jacob W Myers, Woo Yong Park, Heather G Bryant, Alex M Eddie, Genesis A Wilson, Claudia Montufar, Zayedali Shaikh, Zer Vue, Elizabeth R Nunn, Ryoichi Bessho, Matthew A Cottam, Volker H Haase, Antentor O Hinton, Jessica B Spinelli, Jean-Philippe Cartailler, Elma Zaganjor

    Journal of lipid research   65 ( 10 )   100641 - 100641   2024.10

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    A key organismal response to overnutrition involves the development of new adipocytes through the process of adipogenesis. Preadipocytes sense changes in the systemic nutrient status and metabolites can directly modulate adipogenesis. We previously identified a role of de novo nucleotide biosynthesis in adipogenesis induction, whereby inhibition of nucleotide biosynthesis suppresses the expression of the transcriptional regulators PPARγ and C/EBPα. Here, we set out to identify the global transcriptomic changes associated with the inhibition of nucleotide biosynthesis. Through RNA sequencing (RNAseq), we discovered that mitochondrial signatures were the most altered in response to inhibition of nucleotide biosynthesis. Blocking nucleotide biosynthesis induced rounded mitochondrial morphology, and altered mitochondrial function, and metabolism, reducing levels of tricarboxylic acid cycle intermediates, and increasing fatty acid oxidation (FAO). The loss of mitochondrial function induced by suppression of nucleotide biosynthesis was rescued by exogenous expression of PPARγ. Moreover, inhibition of FAO restored PPARγ expression, mitochondrial protein expression, and adipogenesis in the presence of nucleotide biosynthesis inhibition, suggesting a regulatory role of nutrient oxidation in differentiation. Collectively, our studies shed light on the link between substrate oxidation and transcription in cell fate determination.

    DOI： 10.1016/j.jlr.2024.100641

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  • メディカルスタッフの現状と課題 糖尿病チーム医療,資格取得,学会発表,臨床研究,論文投稿,ジェンダー

    佐藤 麻子, 川浪 大治, 藤川 るみ, 菅沼 由美, 古橋 眞人, 森野 勝太郎, 山本 恭子, 和田 幹子, 井町 仁美, 岡田 由紀子, 川崎 麻紀, 近藤 敬一, 笹岡 利安, 高橋 倫子, 富樫 優, 中島 華子, 橋本 尚子, 藤本 啓, 別所 瞭一, 的場 ゆか, 宮 愛香, 安孫子 亜津子, 糖尿病医療者・研究者のダイバーシティをpromoteする委員会

    糖尿病   66 ( 1 )   118 - 128   2023.1

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  • A maternal high-fat diet induces fetal origins of NASH-HCC in mice. International journal

    Takao Takiyama, Toshihiro Sera, Masanori Nakamura, Masato Hoshino, Kentaro Uesugi, Shin-Ichi Horike, Makiko Meguro-Horike, Ryoichi Bessho, Yuri Takiyama, Hiroya Kitsunai, Yasutaka Takeda, Kazuki Sawamoto, Naoto Yagi, Yuji Nishikawa, Yumi Takiyama

    Scientific reports   12 ( 1 )   13136 - 13136   2022.7

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    Maternal overnutrition affects offspring susceptibility to nonalcoholic steatohepatitis (NASH). Male offspring from high-fat diet (HFD)-fed dams developed a severe form of NASH, leading to highly vascular tumor formation. The cancer/testis antigen HORMA domain containing protein 1 (HORMAD1), one of 146 upregulated differentially expressed genes in fetal livers from HFD-fed dams, was overexpressed with hypoxia-inducible factor 1 alpha (HIF-1alpha) in hepatoblasts and in NASH-based hepatocellular carcinoma (HCC) in offspring from HFD-fed dams at 15 weeks old. Hypoxia substantially increased Hormad1 expression in primary mouse hepatocytes. Despite the presence of three putative hypoxia response elements within the mouse Hormad1 gene, the Hif-1alpha siRNA only slightly decreased hypoxia-induced Hormad1 mRNA expression. In contrast, N-acetylcysteine, but not rotenone, inhibited hypoxia-induced Hormad1 expression, indicating its dependency on nonmitochondrial reactive oxygen species production. Synchrotron-based phase-contrast micro-CT of the fetuses from HFD-fed dams showed significant enlargement of the liver accompanied by a consistent size of the umbilical vein, which may cause hypoxia in the fetal liver. Based on these findings, a maternal HFD induces fetal origins of NASH/HCC via hypoxia, and HORMAD1 is a potential therapeutic target for NASH/HCC.

    DOI： 10.1038/s41598-022-17501-8

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  • A case of insulinoma diagnosed postpartum with hypoglycemic symptoms that were masked during pregnancy. International journal

    Tomoe Abe, Yasutaka Takeda, Takao Takiyama, Ayaka Sasaki, Ryoichi Bessho, Mao Sato, Hiroya Kitsunai, Hidemitsu Sakagami, Atsuko Abiko, Koji Imai, Sayaka Yuzawa, Mishie Tanino, Yumi Takiyama

    Clinical case reports   9 ( 4 )   1991 - 1998   2021.4

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    The diagnosis of insulinoma in perinatal women can be difficult, as hypoglycemic symptoms may be masked by pregnancy-associated insulin resistance. In addition, when multiple insulinomas are observed, it is necessary to consider the possibility not only of MEN1, but also of insulinomatosis.

    DOI： 10.1002/ccr3.3924

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  • Establishment of novel specific assay for short-form glucose-dependent insulinotropic polypeptide and evaluation of its secretion in nondiabetic subjects. International journal

    Yasutaka Takeda, Yukihiro Fujita, Tsuyoshi Yanagimachi, Nobuhiro Maruyama, Ryoichi Bessho, Hidemitsu Sakagami, Jun Honjo, Hiroki Yokoyama, Masakazu Haneda

    Physiological reports   8 ( 11 )   e14469   2020.6

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    The short-form glucose-dependent insulinotropic polypeptide (GIP) (1-30) is released from islet alpha cells and promotes insulin secretion in a paracrine manner in vitro. However, it is not well elucidated how GIP (1-30) is involved in glucose metabolism in vivo, since a specific assay system for GIP (1-30) has not yet been established. We first developed a sandwich enzyme-linked immunosorbent assay (ELISA) specific for GIP (1-30) by combining a novel antibody specific to the GIP (1-30) C terminus with the common antibody against GIP N terminus. Then, we explored cross-reactivities with incretins and glucagon-related peptides in this ELISA. GIP (1-30) amide, but not GIP (1-42), GLP-1, or glucagon increased absorbance in a dose-dependent manner. We next measured plasma GIP (1-30) concentrations in nondiabetic participants (ND) during a 75-g oral glucose tolerance test or cookie meal test (carbohydrates 75 g, lipids 28.5 g, proteins 8.5 g). Both glucose and cookie load increased GIP (1-30) concentrations in ND, but the increases were much lower than those of GIP (1-42). Furthermore, the DPP-4 inhibitor significantly increased GIP (1-30) concentrations similarly to GIP (1-42) in ND. In conclusion, we for the first time developed an ELISA specific for GIP (1-30) and revealed its secretion in ND.

    DOI： 10.14814/phy2.14469

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  • Increment of plasma glucose by exogenous glucagon is associated with present and future renal function in type 2 diabetes:a retrospective study from glucagon stimulation test. International journal

    Yasutaka Takeda, Yukihiro Fujita, Ryoichi Bessho, Mao Sato, Tomoe Abe, Tsuyoshi Yanagimachi, Hidemitsu Sakagami, Atsuko Abiko, Yumi Takiyama, Tsuguhito Ota, Masakazu Haneda

    BMC endocrine disorders   19 ( 1 )   99 - 99   2019.10

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    BACKGROUND: Glucagon stimulation test (GST) is often employed to assess the insulin reserve of the pancreatic beta cells in diabetic subjects. The clinical significance of the increment of plasma glucose (Δglucose) by exogenous glucagon during GST has not been elucidated. We investigated the relationship between Δglucose and clinical parameters including the liver and renal function in type 2 diabetic subjects, since we hypothesized that Δglucose is associated with the liver and renal function reflecting the capacity for gluconeogenesis in the organs. METHODS: A total of 209 subjects with type 2 diabetes who underwent GST during admission were included in this cross-sectional study. We defined the difference between plasma glucose at fasting and 6 min after intravenous injection of 1 mg glucagon as Δglucose. We assessed correlations between Δglucose and clinical parameters such as diabetic duration, BMI, HbA1c, beta cell function, serum free fatty acids (FFA) which is known to stimulate gluconeogenesis, liver function, the indices of liver function, renal function, and urinary albumin excretion (UAE). RESULTS: In correlation analysis, Δglucose positively correlated to FFA and estimated glomerular filtration rate (eGFR), but inversely to serum creatinine and cystatin C, although Δglucose showed no correlation with both liver function and the indices of residual liver function. Multiple regression analysis revealed that Δglucose was an independent determinant for the eGFR after 1 year, equally BMI, HbA1c, serum lipids, and UAE, which are known as the predictors for the development of chronic kidney disease. CONCLUSION: Our results suggest that Δglucose during GST might be related to gluconeogenesis in the kidney and could be the determinant of future renal function in type 2 diabetes.

    DOI： 10.1186/s12902-019-0428-6

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  • Hypoxia-inducible factor-1α is the therapeutic target of the SGLT2 inhibitor for diabetic nephropathy. International journal

    Ryoichi Bessho, Yumi Takiyama, Takao Takiyama, Hiroya Kitsunai, Yasutaka Takeda, Hidemitsu Sakagami, Tsuguhito Ota

    Scientific reports   9 ( 1 )   14754 - 14754   2019.10

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    Previous studies have demonstrated intrarenal hypoxia in patients with diabetes. Hypoxia-inducible factor (HIF)-1 plays an important role in hypoxia-induced tubulointerstitial fibrosis. Recent clinical trials have confirmed the renoprotective action of SGLT2 inhibitors in diabetic nephropathy. We explored the effects of an SGLT2 inhibitor, luseogliflozin on HIF-1α expression in human renal proximal tubular epithelial cells (HRPTECs). Luseogliflozin significantly inhibited hypoxia-induced HIF-1α protein expression in HRPTECs. In addition, luseogliflozin inhibited hypoxia-induced the expression of the HIF-1α target genes PAI-1, VEGF, GLUT1, HK2 and PKM. Although luseogliflozin increased phosphorylated-AMP-activated protein kinase α (p-AMPKα) levels, the AMPK activator AICAR did not changed hypoxia-induced HIF-1α expression. Luseogliflozin suppressed the oxygen consumption rate in HRPTECs, and subsequently decreased hypoxia-sensitive dye, pimonidazole staining under hypoxia, suggesting that luseogliflozin promoted the degradation of HIF-1α protein by redistribution of intracellular oxygen. To confirm the inhibitory effect of luseogliflozin on hypoxia-induced HIF-1α protein in vivo, we treated male diabetic db/db mice with luseogliflozin for 8 to 16 weeks. Luseogliflozin attenuated cortical tubular HIF-1α expression, tubular injury and interstitial fibronectin in db/db mice. Together, luseogliflozin inhibits hypoxia-induced HIF-1α accumulation by suppressing mitochondrial oxygen consumption. The SGLT2 inhibitors may protect diabetic kidneys by therapeutically targeting HIF-1α protein.

    DOI： 10.1038/s41598-019-51343-1

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  • 妊娠中の明らかな糖尿病の診断を契機に副腎性Cushing症候群の診断に至った1例

    竹田 安孝, 阿部 智絵, 安孫子 亜津子, 別所 瞭一, 酒井 健太郎, 中村 知伸, 柳町 剛司, 坂上 英充, 藤田 征弘, 滝山 由美, 上田 寛人, 千石 一雄, 太田 嗣人

    糖尿病と妊娠   19 ( 1 )   48 - 53   2019.3

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  • 臨床経過、関連合併症が著明に異なるミトコンドリア糖尿病の同胞例

    阿部 智絵, 竹田 安孝, 別所 瞭一, 酒井 健太郎, 中村 知伸, 柳町 剛司, 坂上 英充, 藤田 征弘, 安孫子 亜津子, 滝山 由美, 太田 嗣人

    糖尿病   62 ( 3 )   162 - 169   2019.3

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  • Impacts of Diabetes and an SGLT2 Inhibitor on the Glomerular Number and Volume in db/db Mice, as Estimated by Synchrotron Radiation Micro-CT at SPring-8. International journal

    Yumi Takiyama, Toshihiro Sera, Masanori Nakamura, Kanaki Ishizeki, Yasuaki Saijo, Tsuyoshi Yanagimachi, Manami Maeda, Ryoichi Bessho, Takao Takiyama, Hiroya Kitsunai, Hidemitsu Sakagami, Daisuke Fujishiro, Yukihiro Fujita, Yuichi Makino, Atsuko Abiko, Masato Hoshino, Kentaro Uesugi, Naoto Yagi, Tsuguhito Ota, Masakazu Haneda

    EBioMedicine   36   329 - 346   2018.10

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    BACKGROUND: Recent large-scale clinical studies demonstrate that sodium-glucose cotransporter 2 (SGLT2) inhibitors protect the diabetic kidney. However, clinical and animal studies have not shown the changes of the total glomeruli in the whole kidney treated with SGLT2 inhibitors. METHODS: We performed computed tomography (CT) imaging on mice using synchrotron radiation to investigate the impact of luseogliflozin, a SGLT2 inhibitor, on the number and volume of glomeruli in the whole kidney. FINDINGS: We did not observe a significant difference in the total glomerular number (Nglom) among mice. Luseogliflozin redistributed the number of glomeruli in different regions, accompanied by the normalization of diabetes-augmented renal volume (Vkidney). Diabetic db/db mice had a larger glomerular volume in the mid-cortex than did control db/m mice, and luseogliflozin increased the glomerular volume in all renal cortical zones of the whole kidney in db/db mice. According to the multivariate regression analysis, hemoglobin A1c level was the most relevant determinant of Vkidney, not Nglom or mean glomerular volume (Vglom), indicating that hyperglycemia induced renal (tubular) hypertrophy, but not glomerular enlargement. Luseogliflozin increased hypoxia in the juxtamedullary region, sustained upregulated renal renin expression and plasma renin activity, and failed to decrease albuminuria by downregulating megalin in db/db mice. INTERPRETATION: Based on our findings, SGLT2 inhibitors may alter glomerular distribution and size in addition to their glucose-lowering effects, presumably by affecting oxygen metabolism and humoral factors. FUND: Funding for this research was provided by The Japan Society for the Promotion of Science, the Japan Diabetes Foundation, and Asahikawa Medical University.

    DOI： 10.1016/j.ebiom.2018.09.048

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  • Development of a Standardized Method for Ex Vivo Respirometry in Intact Kidney Tissue to Assess Regional Metabolism

    Ryoichi Bessho, Volker H. Haase

    JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY   36 ( 10 )   2025.10

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  • Alternative Oxidase Expression Restores Kidney Progenitor Differentiation in Mice with Mitochondrial Complex lll Disruption

    Ryoichi Bessho, Hanako Kobayashi, Volker H. Haase

    JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY   35 ( 10 )   2024.10

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    DOI： 10.1681/ASN.2024fdebyz0j

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  • Renal Proximal Tubular Metallothionein 3 Contributes to Diabetic Kidney Lesion

    Yuri Takiyama, Takao Takiyama, Ryoichi Bessho, Hiroya Kitsunai, Yumi Takiyama

    DIABETES   72   2023.6

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    DOI： 10.2337/db23-398-P

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  • Fetal Renal Hypoxia Response to Maternal Overnutrition

    Takao Takiyama, Yuri Takiyama, Ryoichi Bessho, Hiroya Kitsunai, Yumi Takiyama

    DIABETES   72   2023.6

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    DOI： 10.2337/db23-11-OR

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    日本内分泌学会雑誌   98 ( 2 )   570 - 570   2022.10

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    糖尿病   65 ( Suppl.1 )   S - 245   2022.4

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  • 2型糖尿病におけるアログリプチン/メトホルミン配合錠とビルダグリプチン/メトホルミン配合錠の有効性に関する比較検討

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    糖尿病   65 ( Suppl.1 )   S - 220   2022.4

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    糖尿病   65 ( Suppl.1 )   S - 183   2022.4

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    日本内分泌学会雑誌   97 ( 4 )   659 - 659   2021.12

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  • 中枢性尿崩症(CDI)と重症成人成長ホルモン分泌不全症(GHD)を呈した中枢神経サルコイドーシスの1例

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    日本内分泌学会雑誌   97 ( 4 )   658 - 658   2021.12

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  • 膵性脂肪織炎を併発した糖尿病ケトアシドーシスの一例

    竹田 安孝, 滝山 侑里, 滝山 貴央, 佐々木 彩華, 別所 瞭一, 橘内 博哉, 滝山 由美

    日本内分泌学会雑誌   97 ( 2 )   554 - 554   2021.10

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  • 腎症(基礎) Nrf2活性化剤スルフォラファンは近位尿細管細胞のTFAMを活性化しSTINGを抑制する

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    糖尿病合併症   35 ( Suppl.1 )   177 - 177   2021.9

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  • がん 胎生期過栄養誘発NAFLD関連肝癌 HIF-1α/HORMAD1 pathwayの役割

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    糖尿病合併症   35 ( Suppl.1 )   180 - 180   2021.9

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  • ACTH産生前立腺小細胞癌の1例

    宮内 琴菜, 渡邊 成樹, 堀 淳一, 和田 直樹, 玉木 岳, 北 雅史, 柿崎 秀宏, 佐藤 茉欧, 別所 瞭一, 竹田 安孝, 滝山 由美, 長門 利純, 小林 博也

    泌尿器外科   34 ( 臨増 )   782 - 782   2021.6

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  • HORMAD1, a Novel Hypoxia-Inducible Factor-1 Target, Is Upregulated in Maternal Overnutrition-Induced Nonalcoholic Steatohepatitis (NASH)/Hepatocellular Carcinoma

    Takao Takiyama, Ryoichi Bessho, Hiroya Kitsunai, Yasutaka Takeda, Hidemitsu Sakagami, Toshihiro Sera, Masanori Nakamura, Shin-Ichi Horike, Yuji Nishikawa, Yumi Takiyama

    DIABETES   70   2021.6

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    DOI： 10.2337/db21-1171-P

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  • The Nrf2 Activator Increases TFAM and Suppresses STING in Human Renal Proximal Tubular Cells

    Ryoichi Bessho, Takao Takiyama, Suratsawadee Promsuwan, Hiroya Kitsunai, Kazuki Sawamoto, Yasutaka Takeda, Yumi Takiyama

    DIABETES   70   2021.6

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    DOI： 10.2337/db21-391-P

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  • Nrf2活性化剤によるTFAM活性化とSTING抑制作用

    別所 瞭一, 滝山 貴央, Promsuwan Suratsawadee, 宿田 夕季, 橘内 博哉, 澤本 一樹, 竹田 安孝, 坂上 英充, 滝山 由美

    糖尿病   64 ( Suppl.1 )   I - 3   2021.5

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  • 胎生期過栄養によるNASH肝細胞癌発生機序の検討

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    糖尿病   64 ( Suppl.1 )   P - 1   2021.5

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    日本内分泌学会雑誌   96 ( 4 )   987 - 987   2021.4

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    日本内分泌学会雑誌   96 ( 3 )   596 - 596   2021.1

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  • 腎症 放射光CTイメージングによる1型糖尿病モデルマウス糸球体評価

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    糖尿病合併症   34 ( Suppl.1 )   229 - 229   2020.11

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  • 血糖管理 ヒトにおける'short-form'GIPの分泌動態の検証と臨床的意義の解明

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  • Gitelman症候群あるいは3型Bartter症候群が疑われた一例

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  • 前立腺癌による異所性ACTH症候群の剖検例

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    日本内分泌学会雑誌   96 ( 1 )   288 - 288   2020.8

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  • 分娩直後から低血糖の顕在化がみられ、診断に至ったインスリノーマの一例

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    日本内分泌学会雑誌   96 ( 1 )   332 - 332   2020.8

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  • 正常耐糖能者におけるshort-form GIPの分泌動態に関する検証

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    日本内分泌学会雑誌   96 ( 1 )   302 - 302   2020.8

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  • 胎生期高脂肪食誘発性脂肪肝炎 肝癌モデルマウスの確立

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    糖尿病   63 ( Suppl.1 )   S - 342   2020.8

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  • ガドリニウム造影剤を用いた静脈サンプリングが局在診断に有用であった原発性副甲状腺機能亢進症の一例

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    日本内分泌学会雑誌   96 ( 1 )   279 - 279   2020.8

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  • Maternal Overnutrition Causes DNA Alkylation in Fetal Liver, Suppresses FasL, and Upregulates HIF-1 Signaling Pathway in Neonatal Liver in Nonalcoholic Steatohepatitis (NASH)-Based Hepatocellular Carcinoma in Offspring

    Takao Takiyama, Ryoichi Bessho, Kazuki Sawamoto, Yumi Takiyama

    DIABETES   69   2020.6

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    DOI： 10.2337/db20-1845-P

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  • A型インフルエンザ感染症が誘因と考えられた糖尿病ケトアシドーシス(DKA)の1例

    佐々木 彩華, 別所 瞭一, 佐藤 茉欧, 阿部 智絵, 橘内 博哉, 竹田 安孝, 坂上 英充, 安孫子 亜津子, 滝山 由美, 太田 嗣人

    糖尿病   63 ( 5 )   350 - 350   2020.5

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  • 糖尿病ケトアシドーシス(DKA)に急性腎障害(AKI)を併発した急性発症1型糖尿病の1例

    福山 茉莉花, 佐々木 彩華, 別所 瞭一, 佐藤 茉欧, 阿部 智絵, 橘内 博哉, 竹田 安孝, 坂上 英充, 安孫子 亜津子, 滝山 由美, 太田 嗣人

    糖尿病   63 ( 5 )   350 - 350   2020.5

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  • ヒトにおけるshort-form GIPの分泌動態に関する検討

    竹田 安孝, 藤田 征弘, 柳町 剛司, 丸山 順裕, 本庄 潤, 横山 宏樹, 別所 瞭一, 坂上 英充, 羽田 勝計, 太田 嗣人

    日本内科学会雑誌   109 ( 臨増 )   167 - 167   2020.2

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  • インスリン療法中の低血糖を契機に副腎不全症が顕在化し、診断に至ったIgG4関連下垂体炎の1例

    阿部 智絵, 竹田 安孝, 佐々木 彩華, 別所 瞭一, 佐藤 茉欧, 橘内 博哉, 坂上 英充, 安孫子 亜津子, 滝山 由美, 太田 嗣人

    日本内分泌学会雑誌   95 ( 3 )   868 - 868   2020.1

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  • 非特異的症候の顕在化を契機に診断に至ったCushing病の1例

    滝山 貴央, 竹田 安孝, 別所 瞭一, 佐藤 茉欧, 阿部 智絵, 橘内 博哉, 坂上 英充, 安孫子 亜津子, 滝山 由美, 太田 嗣人

    日本内分泌学会雑誌   95 ( 2 )   708 - 708   2019.10

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  • A Novel Renoprotective Target of SGLT2 Inhibitor: HIF-1α Inhibition and AMPK Activation in Renal Proximal Tubular Epithelial Cells

    Ryoichi Bessho, Yumi Takiyama, Takao Takiyama, Tsuguhito Ota

    DIABETES   68   2019.6

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    DOI： 10.2337/db19-492-P

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  • Secretion of the Short-Form Gastric Inhibitory Polypeptide in Nondiabetic and Diabetic Subjects

    Yasutaka Takeda, Yukihiro Fujita, Tsuyoshi Yanagimachi, Nobuhiro Maruyama, Ryoichi Bessho, Hidemitsu Sakagami, Masakazu Haneda, Tsuguhito Ota

    DIABETES   68   2019.6

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    DOI： 10.2337/db19-1948-P

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  • Synchrotron Radiation Micro-CT Reveals Glomerular Loss without Glomerular or Renal Hypertrophy in Streptozotocin-Induced Type 1 Diabetic Mice

    Yumi Takiyama, Toshihiro Sera, Masanori Nakamura, Ryoichi Bessho, Takao Takiyama, Tsuguhito Ota, Masakazu Haneda

    DIABETES   68   2019.6

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    DOI： 10.2337/db19-493-P

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  • 妊娠糖尿病における妊娠中・分娩時の血糖管理と新生児低血糖との関連性

    阿部 智絵, 安孫子 亜津子, 佐々木 彩華, 別所 瞭一, 佐藤 茉欧, 中村 知伸, 柳町 剛司, 橘内 博哉, 竹田 安孝, 坂上 英充, 滝山 由美, 太田 嗣人

    糖尿病   62 ( Suppl.1 )   S - 282   2019.4

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  • SGLT2阻害薬の新規腎保護作用機構 ミトコンドリア酸素消費抑制を介したHIF-1α蛋白発現抑制とAMPK活性化

    別所 瞭一, 滝山 由美, 太田 嗣人

    糖尿病   62 ( Suppl.1 )   S - 203   2019.4

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  • short-form GIPの測定系の確立とヒトにおける分泌動態の検討

    竹田 安孝, 藤田 征弘, 柳町 剛司, 丸山 順裕, 本庄 潤, 横山 宏樹, 別所 瞭一, 坂上 英充, 羽田 勝計, 太田 嗣人

    糖尿病   62 ( Suppl.1 )   S - 331   2019.4

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  • 原発性アルドステロン症とsubclinical Cushing病による二次性低K性周期性四肢麻痺と考えられた1例

    竹田 安孝, 佐々木 彩華, 別所 瞭一, 佐藤 茉欧, 阿部 智絵, 中村 知伸, 柳町 剛司, 橘内 博哉, 坂上 英充, 藤田 征弘, 安孫子 亜津子, 滝山 由美, 太田 嗣人

    日本内分泌学会雑誌   94 ( 3 )   734 - 734   2018.12

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  • 緩徐進行1型糖尿病と考えられたovert diabetes in pregnancyの1例

    阿部 智絵, 竹田 安孝, 佐々木 彩華, 別所 瞭一, 佐藤 茉欧, 中村 知伸, 柳町 剛司, 橘内 博哉, 坂上 英充, 藤田 征弘, 安孫子 亜津子, 滝山 由美, 太田 嗣人

    糖尿病と妊娠   18 ( 3 )   S - 96   2018.11

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  • Luseogliflozin Inhibits HIF-1α Expression in Renal Proximal Tubular Epithelial Cells

    Ryoichi Bessho, Yumi Takiyama, Tsuguhito Ota

    DIABETES   67   2018.7

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    DOI： 10.2337/db18-90-OR

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  • レセプター結合に基づくbioassay法による活性型インクレチン及グルカゴン測定の有用性の検討

    柳町 剛司, 藤田 征弘, 本庄 潤, 竹田 安孝, 坂上 英充, 別所 瞭一, 滝山 由美, 安孫子 亜津子, 横山 宏樹, 太田 嗣人, 羽田 勝計

    糖尿病   61 ( Suppl.1 )   S - 322   2018.4

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  • インスリノーマとガストリノーマが併存した透析期慢性腎不全の1例

    竹田 安孝, 別所 瞭一, 酒井 健太郎, 阿部 智絵, 中村 知伸, 柳町 剛司, 坂上 英充, 藤田 征弘, 安孫子 亜津子, 滝山 由美, 太田 嗣人

    日本内分泌学会雑誌   94 ( 1 )   448 - 448   2018.4

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  • 不妊治療における体外受精・胚移植直後、再燃したバセドウ病の一例

    藤田 征弘, 別所 瞭一, 酒井 健太郎, 中村 知伸, 阿部 智絵, 柳町 剛司, 竹田 安孝, 坂上 英充, 安孫子 亜津子, 牧野 雄一, 太田 嗣人

    日本内分泌学会雑誌   94 ( 1 )   388 - 388   2018.4

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  • SGLT2阻害薬ルセオグリフロジンは、近位尿細管細胞における低酸素誘導HIF-1発現を抑制する

    別所 瞭一, 滝山 由美, 酒井 健太郎, 阿部 智絵, 中村 知伸, 柳町 剛司, 竹田 安孝, 坂上 英充, 藤田 征弘, 安孫子 亜津子, 太田 嗣人

    糖尿病   61 ( Suppl.1 )   S - 383   2018.4

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  • overt diabetes in pregnancyを契機に副腎性Cushing症候群と診断した一例

    別所 瞭一, 竹田 安孝, 酒井 健太郎, 阿部 智絵, 中村 知伸, 柳町 剛司, 坂上 英充, 藤田 征弘, 安孫子 亜津子, 滝山 由美, 太田 嗣人

    日本内分泌学会雑誌   94 ( 1 )   414 - 414   2018.4

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  • 血糖コントロール目的に入院した糖尿病網膜症合併患者に関する検討

    酒井 健太郎, 別所 瞭一, 阿部 智恵, 中村 知伸, 竹田 安孝, 坂上 英充, 藤田 征弘, 安孫子 亜津子

    糖尿病   61 ( 3 )   150 - 150   2018.3

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  • 異なる臨床経過を辿ったミトコンドリア糖尿病の同胞例

    阿部 智絵, 別所 瞭一, 酒井 健太郎, 中村 知伸, 柳町 剛司, 竹田 安孝, 坂上 英充, 藤田 征弘, 滝山 由美, 安孫子 亜津子, 牧野 雄一

    糖尿病   61 ( 3 )   148 - 148   2018.3

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  • C型慢性肝炎に対する直接作用型抗ウイルス薬治療後、血糖改善を呈した2型糖尿病の1症例

    滝山 由美, 別所 瞭一, 酒井 健太郎, 阿部 智恵, 中村 知伸, 竹田 安孝, 坂上 英充, 藤田 征弘, 安孫子 亜津子

    糖尿病   61 ( 3 )   144 - 144   2018.3

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  • 持続皮下インスリン注入療法患者のシックデイ時に発症した糖尿病性ケトアシドーシス

    橋本 茉弥, 別所 瞭一, 酒井 健太郎, 阿部 智絵, 中村 知伸, 竹田 安孝, 坂上 英充, 本庄 潤, 藤田 征弘, 安孫子 亜津子

    糖尿病   61 ( 3 )   149 - 149   2018.3

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  • 妊娠中のovert diabetes in pregnancyを契機に、副腎性クッシング症候群と診断した一例

    竹田 安孝, 阿部 智絵, 安孫子 亜津子, 別所 瞭一, 酒井 健太郎, 中村 知伸, 柳町 剛史, 坂上 英充, 藤田 征弘, 滝山 由美, 上田 寛人, 千石 一雄

    糖尿病と妊娠   17 ( 3 )   S - 81   2017.11

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  • SGLT2 Inhibitor Therapy Improves Blood Glucose but Does Not Prevent Albuminuria nor Glomerular Hypertrophy in Diabetic db/db Mice

    Yumi Takiyama, Toshihiro Sera, Masanori Nakamura, Tsuyoshi Yanagimachi, Ryoichi Bessho, Yukihiro Fujita, Masato Hoshino, Kentaro Uesugi, Yasuaki Saijo, Naoto Yagi, Masakazu Haneda

    DIABETES   66   A134 - A134   2017.6

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  • モデル動物 新規糖尿病腎症モデル 低酸素誘導抗酸化物質Metallothionein3トランスジェニックマウス

    滝山 由美, 別所 瞭一, 藤田 征弘, 安孫子 亜津子, 立野 正敏, 仲川 孝彦, 羽田 勝計

    糖尿病合併症   30 ( Suppl.1 )   193 - 193   2016.9

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  • 上行結腸癌の一例

    別所 瞭一, 坂下 建人, 玉川 進

    旭川医療センター医学雑誌   2   48 - 51   2016.7

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  • 内視鏡的に治療し得た拍動性血管瘤様の大腸Angiodysplasiaの一例

    別所 瞭一, 斉藤 裕樹, 高添 愛, 横浜 吏郎, 柏谷 朋, 平野 史倫, 安部 茂, 松本 学也, 辻 忠克, 安尾 和裕, 西村 英夫

    旭川医療センター医学雑誌   2   29 - 31   2016.7

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  • 一過性脳虚血発作を発症後、呼吸不全の急速な悪化により死亡した間質性肺炎の一例

    別所 瞭一, 藤内 智, 玉川 進

    旭川医療センター医学雑誌   2   45 - 47   2016.7

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  • 急激な転帰を辿った重症急性膵炎の一例

    別所 瞭一

    旭川医療センター医学雑誌   2   33 - 36   2016.7

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  • Zinc; HIF-1 Mimetic in Human Renal Proximal Tubular Cells

    Ryoichi Bessho, Yumi Takiyama, Manami Maeda, Kuralay K. Atageldiyeva, Yukihiro Fujita, Masakazu Haneda

    DIABETES   65   A137 - A137   2016.6

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  • ヒト近位尿細管細胞において、亜鉛はTGF-β1誘導線維化を抑制し、HIF-1 target遺伝子発現を増強する

    別所 瞭一, 前田 愛実, 滝山 由美, Atageldiyeva Kralay K., 柳町 剛司, 長南 茉欧, 高橋 耕平, 酒井 健太郎, 中村 知伸, 永島 優樹, 竹田 安孝, 辻 賢, 本庄 潤, 藤田 征弘, 安孫子 亜津子, 羽田 勝計

    糖尿病   59 ( Suppl.1 )   S - 161   2016.4

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  • 糖尿病腎症 ヒト糖尿病性腎症近位尿細管における抗酸化物質Metallothionein3の発現制御機構の検討

    滝山 由美, 別所 瞭一, 柳町 剛司, 本庄 潤, 藤田 征弘, 羽田 勝計

    糖尿病合併症   29 ( Suppl.1 )   138 - 138   2015.11

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  • 持続的血液濾過透析により救命し得たメトホルミンによる乳酸アシドーシスの一例

    別所 瞭一, 中嶋 駿介, 鷹架 健一, 林 健太郎, 長島 道生, 西浦 猛, 小林 厚志, 岡田 基, 小北 直宏, 藤田 智

    日本救急医学会雑誌   26 ( 8 )   342 - 342   2015.8

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  • SGLT2 Inhibitor Luseogliflozin (TS-071) Protects from Diabetic Nephropathy in an Animal Model of Type 2 Diabetes

    Yumi Takiyama, Ryoichi Bessho, Manami Maeda, Kuralay K. Atageldiyeva, Tsuyoshi Yanagimachi, Jun Honjo, Yukihiro Fujita, Yuichi Makino, Masakazu Haneda

    DIABETES   63   A136 - A136   2014.6

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Awards

  • Young Investigator’s Award for Junior Resident (As a Mentor)

    2021   Japanese Society of Internal Medicine (The 292th Hokkaido Regional Meeting)  

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  • Best oral presentation award

    2020   3rd Asia-Pacific CardioMetabolic Syndrome Congress  

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  • Young Investigator’s Award for Junior Resident

    2016   Japanese Society of Internal Medicine (The 277th Hokkaido Regional Meeting)  

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Research Projects

  • Advances in Research Conference Travel Support

    2025.11

    American Society of Nephrology 

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    Authorship：Principal investigator 

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  • Dissecting Mitochondrial Electron Transport Function in Renal Fibrogenesis

    2024.7 - 2026.6

    American Society of Nephrology and KidneyCure Grants  Ben J. Lipps Research Fellowship Program 

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  • Dissection the role of mitochondrial complex III function in diabetic kidney disease

    2023.4 - 2025.3

    The ITO Foundation for the Promotion of Medical Sciences  Research Fellowship 

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  • Dissection the role of mitochondrial electron transport in the pathogenesis of chronic kidney disease

    2023.4 - 2024.3

    The Uehara Memorial Foundation  Postdoctoral Fellowship 

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  • Renoprotective Effect of Glucoraphanin on Diabetic Nephropathy

    2021.10 - 2022.9

    Asahikawa Medical University Fund  Research Support 

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  • Disecting the effect of glucoraphanin, an Nrf2 activator, on diabetic nephropathy.

    Grant number：20K17271  2020.4 - 2023.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Early-Career Scientists

    Bessho Ryoichi

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    Grant amount：\4,290,000 （ Direct Cost: \3,300,000 、 Indirect Cost：\990,000 ）

    NF-E2-related Factor 2 (Nrf2) activators have renoprotective potential, however their mechanisms are not fully elucidated. In this study, we investigated the effect of Glucoraphanin (GR), an Nrf2 activator derived from broccoli sprouts, and its active form, sulforaphane (SFN), on diabetic nephropathy.
    We treated wild-type and Nrf2-deficient (C57BL/6J background) mice, made diabetic by a high-fat diet and low-dose streptozotocin, with a GR containing diet. GR did not affect glomerular lesions and albuminuria, but improved tubular damage and renal fibrosis in both wild-type and Nrf2-deficient diabetic mice.
    GR decreased Sodium-Glucose co-Transporter 2 (SGLT2) protein expression in wild-type and Nrf2-deficient diabetic mice. In addition, SFN showed an Nrf2-independent decrease in SGLT2 gene expression in cultured human proximal tubular epithelial cells. These results suggest that GR may have renoprotective effects in a Nrf2-independent manner, and the involvement of SGLT2 down-regulation.

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  • Effect of Glucoraphanin Extracted from Broccoli Sprouts on Diabetic Nephropathy

    2020.4 - 2021.3

    Mishima Kaiun Memorial Foundation  Research Support 

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  • Hypoxia-inducible factor-1α is the therapeutic target of the SGLT2 inhibitor for diabetic nephropathy.

    2020.2

    3rd Asia-Pacific CardioMetabolic Syndrome Congress  Travel grant 

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  • A case of adrenal Cushing's syndrome manifested as overt diabetes in pregnancy

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  • Luseogliflozin Inhibits HIF-1α Expression in Renal Proximal Tubular Epithelial Cells

    Asahikawa Medical University Foundation  International Conference Travel Grant 

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Teaching Experience

  • Health & Disease Concepts

    2020 - 2023 Institution：Hokuto College of Health and Welfare, Asahikawa

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  • Pathophysiology II

    2017 - 2023 Institution：Asahikawa College of Nursing, Hokkaido

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Academic Activities

  • Peer review for Molecular Biomedicine

    Role(s)： Peer review

    2025.12

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  • Peer review for Molecular Medicine

    Role(s)： Peer review

    2025.1

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  • Peer review for Molecular Biomedicine

    Role(s)： Peer review

    2024.12

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  • Peer review for Molecular Medicine

    Role(s)： Peer review

    2023.12

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  • Peer review for Molecular Medicine

    Role(s)： Peer review

    2023.9

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  • Steering Committee Member, Hokkaido Young Diabetologists' Seminar

    Role(s)： Planning, management, etc.,　Panel moderator, session chair, etc.

    2022.12

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  • 第56回日本糖尿病学会北海道地方会 シンポジウム 『小さなワクワクが開いた扉  ～医療スタッフ優秀演題賞受賞者が伝えたい臨床研究のおもしろさ～』 コーディネーター

    Role(s)： Panel moderator, session chair, etc.

    2022.11

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  • Peer review for Endocrine Journal

    Role(s)： Peer review

    2022.6

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